Alloantigen presentation by ethylcarbodiimide-treated dendritic cells induces T cell hyporesponsiveness, and prolongs organ graft survival

Ethylcarbodiimide (ECDI) couples soluble antigens (Ag) to lymphoid cells bestowing tolerizing potential. We examined whether ECDI-treated allogeneic dendritic cells (DC) could promote Ag-specific T cell unresponsiveness and prolong graft survival. Exposure of murine myeloid DC to ECDI did not affect...

Full description

Saved in:
Bibliographic Details
Published in:Clinical immunology (Orlando, Fla.) Fla.), 2003-09, Vol.108 (3), p.190-198
Main Authors: Kaneko, Katsuhiko, Morelli, Adrian E, Wang, Zhiliang, Thomson, Angus W
Format: Article
Language:English
Subjects:
Animals
Antigen Presentation
Apoptosis
Biological and medical sciences
Cell Division
Clonal Anergy
Cross-Linking Reagents - pharmacology
Cytotoxicity Tests, Immunologic
Dendritic cells
Dendritic Cells - drug effects
Dendritic Cells - immunology
Ethylcarbodiimide
Ethyldimethylaminopropyl Carbodiimide - pharmacology
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Graft Survival - drug effects
Graft Survival - immunology
Heart Transplantation - immunology
Interferon-gamma - biosynthesis
Interleukin-10 - biosynthesis
Interleukin-5 - biosynthesis
Isoantigens - immunology
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C3H
Mice, Inbred C57BL
T cells
T-Lymphocytes - immunology
Tissue, organ and graft immunology
Transplantation
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Ethylcarbodiimide (ECDI) couples soluble antigens (Ag) to lymphoid cells bestowing tolerizing potential. We examined whether ECDI-treated allogeneic dendritic cells (DC) could promote Ag-specific T cell unresponsiveness and prolong graft survival. Exposure of murine myeloid DC to ECDI did not affect surface immunophenotype but reduced their ability to cluster with T cells, enhanced their apoptotic death, and markedly reduced their allostimulatory activity. Anti-donor proliferative and cytotoxic T cell responses of mice primed with ECDI-treated DC were markedly inhibited. Secretion of both Th1 (IFNγ) and Th2 cytokines (IL-5, IL-10) was suppressed. Cardiac allograft survival in mice preconditioned with a single injection of ECDI-DC was prolonged significantly. These results indicate that ECDI-treated DC promote T cell unresponsiveness to donor alloAgs and prolong transplant survival. The effects are not associated with sparing of Th2 responses, but may reflect inhibitory effects of apoptotic donor DC on host immune reactivity.
ISSN:1521-6616
1521-7035
DOI:10.1016/S1521-6616(03)00141-4